You first notice a bump — a tender, cherry red bruise. Over the next 12 hours, the center of this painful spot on your leg becomes dark violet in color. A day later this raised red bump ruptures and fluid oozes forth. I hope you are on the way to the hospital at this point, because flesh-eating bacteria might be running amok in your body.

These microbes have appeared in such films as the late-night scifi flick Cube Zero, in which a prisoner is sprayed with flesh-eating bacteria and melts before the audience's eyes. But does this horrifying bacteria act as quickly as depicted in movies? And more importantly, do the bacteria actually dine on your flesh?

Flesh-eating bacteria formally goes by the mildly less frighting name necrotizing fasciitis in medical circles. Necrotizing fasciitis occurs through a cascading series of events, with the bacteria Clostridium perfringens and Streptococcus pyogenes commonly initiating the infection. The bacteria often enter through an open wound, particularly when the wound is left exposed in a foreign environment like seawater or sewage.

These bacteria lurk in benign places — a 14-year-old in South Carolina contracted the illness in 2009 after removing rocks from the bottom of a local lake. He lost half of his palate, a portion of his nose, and several teeth as surgeons extracted flesh to prevent spreading of the bacteria. In another incident, the guitarist of the venerable thrash metal band Slayer contracted the disease from a spider bite in 2011.

In necrotizing fasciitis, the bacteria doesn't actually eat the flesh of your body. The bacteria sneaking their way into your body spur on the release of proteins, which have a toxic effect in increased quantities. Phospholipase A2 and antigens released by the bacteria enter the cells of your skin, fat, and the connective tissue covering your muscles and begin wreaking havoc. (Here's an image of a necrotizing fasciitis infection, but be forewarned that it's very graphic. Like, Krokodil graphic.)

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Phospholipase A2 is often found in snake venom and bee stings. When excess Phospholipase A2 appears in the body, your cells respond by releasing arachidonic acid. The presence of additional arachidonic acid disrupts cells, causing inflammation and pain. Fortunately, the effects of Phospholipase A2 can act as a warning sign for those with necrotizing fasciitis, hopefully leading an individual to seek out treatment.

The antigens released are commonly a type of superantigen that causes non-specific activation of T-cells, or those cells that are the primary line of defense in your body's immune system. The over-activation of T-cells leads to the release of enormous quantities of cytokines (a small protein) at the infection site. The cytokines start a cell signalling cascade that begins the destruction of tissue cells in the region. The foreign bacteria causing necrotizing fasciitis do not eat your flesh, but they do something a little more sinister — these bacteria turn your flesh against you.

What happens should you contract necrotizing fasciitis? Patients must receive intravenous antibiotics immediately and a series of surgical operations to remove dead tissue. If the operations are unsuccessful and the necrotizing fasciitis is contained to an appendage, amputation of an infected arm or leg is the safest course. Patients with necrotizing fasciitis often undergo hyperbaric oxygen treatment, with the hope that the increased oxygen levels help the body heal.

Several hundred individuals contract necrotizing fasciitis in North America each year. Even with treatment, 25% of patients that contract necrotizing fasciitis die from complications of the disease. Years of skin grafts and pain management follow those who are lucky enough to survive.

Also, an even scarier type of necrotizing fasciitis, Fournier gangrene, targets the perineum, and more specifically, the groin and genitals. Modern cases are not common, but historical autopsies suggest that the Roman emperor Galerius and Herod the Great died of this malady. A 69-year-old Herod suffered from a combination of kidney failure and Fournier gangrene, degrading his flesh to the point that worms and maggots moved in and out of the affected areas freely. Fournier gangrene, when it appears in modern society, carries a 40% mortality rate.